Please use this identifier to cite or link to this item: https://repositorio.unifesp.br/handle/11600/38093
Title: Thyroid hormone interacts with the sympathetic nervous system to modulate bone mass and structure in young adult mice
Authors: Fonseca, Tatiana L.
Teixeira, Marilia B. C. G.
Rodrigues-Miranda, Manuela
Silva, Marcos V.
Martins, Gisele M.
Costa, Cristiane C.
Arita, Danielle Y. [UNIFESP]
Perez, Juliana D. [UNIFESP]
Casarini, Dulce E. [UNIFESP]
Brum, Patricia C.
Gouveia, Cecilia H. A.
Universidade de São Paulo (USP)
Universidade Federal de São Paulo (UNIFESP)
Keywords: thyroid hormone
sympathetic nervous system
bone
alpha-adrenoceptors
beta-adrenoceptors
Issue Date: 15-Aug-2014
Publisher: Amer Physiological Soc
Citation: American Journal of Physiology-endocrinology and Metabolism. Bethesda: Amer Physiological Soc, v. 307, n. 4, p. E408-E418, 2014.
Abstract: To investigate whether thyroid hormone (TH) interacts with the sympathetic nervous system (SNS) to modulate bone mass and structure, we studied the effects of daily T-3 treatment in a supraphysiological dose for 12 wk on the bone of young adult mice with chronic sympathetic hyperactivity owing to double-gene disruption of adrenoceptors that negatively regulate norepinephrine release, alpha(2A)-AR, and alpha(2C)-AR (alpha(2A/2C)-AR(-/-) mice). As expected, T3 treatment caused a generalized decrease in the areal bone mineral density (aBMD) of WT mice (determined by DEXA), followed by deleterious effects on the trabecular and cortical bone microstructural parameters (determined by mu CT) of the femur and vertebra and on the biomechanical properties (maximum load, ultimate load, and stiffness) of the femur. Surprisingly, alpha(2A/2C)-AR(-/-) mice were resistant to most of these T-3-induced negative effects. Interestingly, the mRNA expression of osteoprotegerin, a protein that limits osteoclast activity, was upregulated and downregulated by T-3 in the bone of alpha(2A/2C)-AR(-/-) and WT mice, respectively. beta(1)-AR mRNA expression and IGF-I serum levels, which exert bone anabolic effects, were increased by T-3 treatment only in alpha(2A/2C)-AR(-/-) mice. As expected, T-3 inhibited the cell growth of calvaria-derived osteoblasts isolated from WT mice, but this effect was abolished or reverted in cells isolated from KO mice. Collectively, these findings support the hypothesis of a TH-SNS interaction to control bone mass and structure of young adult mice and suggests that this interaction may involve alpha(2)-AR signaling. Finally, the present findings offer new insights into the mechanisms through which TH regulates bone mass, structure, and physiology.
URI: http://repositorio.unifesp.br/handle/11600/38093
ISSN: 0193-1849
Other Identifiers: http://dx.doi.org/10.1152/ajpendo.00643.2013
Appears in Collections:Em verificação - Geral

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